Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 2008;51:179-181
Published online before print December 24, 2007, doi: 10.1161/HYPERTENSIONAHA.107.100222
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
51/2/179    most recent
HYPERTENSIONAHA.107.100222v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by de Simone, G.
Right arrow Articles by Devereux, R. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by de Simone, G.
Right arrow Articles by Devereux, R. B.
Related Collections
Right arrow Cardio-renal physiology/pathophysiology
Right arrow Contractile function
Right arrow Hypertrophy
Right arrowRelated Article

(Hypertension. 2008;51:179.)
© 2008 American Heart Association, Inc.


Editorial Commentaries

Assessing Left Ventricular Performance

A Rashomon Effect

Giovanni de Simone; Richard B. Devereux

From Department of Clinical and Experimental Medicine (G.d.S.), Federico II University, Naples, Italy; and Weill-Cornell Medical College (R.B.D.), New York, NY.

Correspondence to Giovanni de Simone, Department of Clinical and Experimental Medicine, Federico II University Hospital, v.S.Pansini 5, 80131 Naples, Italy. E-mail simogi@unina.it


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 


*    Introduction
 
The physiology of conduit arteries can be approximated noninvasively. One simple method to estimate arterial load is by computation of effective arterial elastance (Ea). Ea incorporates the steady component (peripheral resistance) and the pulsatile components of arterial load, including total arterial compliance and aortic characteristic impedance. Invasive studies and simulations have shown that Ea can be approximated by the ratio of left ventricular (LV) end-systolic pressure to stroke volume in normal and hypertensive human subjects.1,2 An important practical advantage of the calculation of Ea is the merging of all components of arterial load into a single quantitative variable, although it has the limitations of not separating the relative contributions of steady and pulsatile components2 and of relative sensitivity to variation of heart rate.3

Ea influences stroke volume and is related to LV contractility, as assessed at end ejection by the pressure-volume loop and determination of the LV elastance (Emax).4,5 Thus, Ea has been combined with Emax, the slope of a regression line connecting end-systolic pressures and volumes obtained at different loading conditions. The ratio Ea/Emax is widely used as a measure of LV-arterial coupling. As emphasized recently by Baicu et al,6 LV function, LV performance, LV contractility, and myocardial contractility are not interchangeable terms. Experimental studies suggest that LV performance, measured as stroke work (SW),6 is maximal when Emax=Ea. LV performance increases its efficiency when, for a given SW, myocardial oxygen consumption is lower. The optimal efficiency of LV performance is achieved at Ea. . . [Full Text of this Article]


Related Article:

Arterioventricular Coupling and Ventricular Efficiency After Antihypertensive Therapy: A Noninvasive Prospective Study
Martin Osranek, John H. Eisenach, Bijoy K. Khandheria, Krishnaswamy Chandrasekaran, James B. Seward, and Marek Belohlavek
Hypertension 2008 51: 275-281. [Abstract] [Full Text] [PDF]